Hypotension and vascular leak are severe and frequently dose-limiting toxicities of IL-2 administration. The mechanisms for IL-2-induced hypotension are beginning to be understood. Nitric oxide production and phospholipase A-2 are thought to be important mediators of hypotension from cytokine administration. Other mechanisms may also be operative in IL-2-induced hypotension and vascular leak. Animal models have shown that IL-2-activated lymphocytes adhere to vascular endothelium and cause vascular leak. TGF-induced hypotension may also be caused by leukocyte-mediated vascular damage. Lymphocyte adhesion and vascular leak can be decreased in a rabbit model by giving intravenous dextrans with a molecular weight of 500,000. Hetastarch is a synthetic amylopectin similar to dextran with a molecular weight of approximately 450,000. It is approved by the FDA for volume resuscitation after trauma. This protocol seeks to determine if hetastarch can decrease lymphocyte adherence to blood vessels and thus prevent IL-2-induced hypotension and vascular leak. 6 pts. with IL-2-induced hypotension requiring phenylephrine at doses greater than 100 mcg/kg/min have received hetastarch. Three of these pts. had an increase of blood pressure that permitted rapid titration off pressor support. Transient elevations of liver function tests, prothrombin times, and partial thromboplatin times were observed. These toxicities have been previously observed with hetastarch administration and were not dose limiting.